Regions where HIV infection is prominent frequently overlap malaria endemic regions. However, the impact of coinfection with HIV and malaria is not clear. We inoculated a monkey with Plasmodium knowlesi. 57 days after SIV inoculation, a time when the SIV infection had already caused a decrease in the percentage of CD4+ cells. Maximum parasitemia (11.6%) occurred 9 days after malaria inoculation andwas treated by chloroquine. After treatment the hematocrit recovered steadily through day 26, when malaria re-emerged and a single chloroquine treatment was given. The parasitemia and accompanying decrease in hematocrit rapidly resolved. Malaria re-emerged on day 46 and was again treated. After this third recrudescence and treatment, the parasite did not reappear, so the monkey was reinoculated with malaria. Nine days later the parasite was detected but did not require treatment, remaining a chronic low level infestation. The coinfection with malaria did not affect the progress of SI V infection. The percentage of cells expressing CD4, CD8, CD2, or CD20 did not differ in the malaria-infected monkey compared to other monkeys inoculated with SIV at the same time. No conclusions can be drawn based on 1 monkey, but the feasibility of the SIV/malaria coinfection has been demonstrated. An additional SIV-infected monkey was recently inoculated with malaria 327 days after SIV, a point when the percentage of CD4+ cells had declined markedly. A naive control monkey was inoculated at the same time. It will be interesting to see if the SIV-infected monkey inoculated with malaria at a much later stage of SIV infection will still be able to contain the parasite after 3 treatments, and to see if the ability to control the parasite differs in the control monkey. FUNDING NIH-N01-AI-65310 PUBLICATIONS NONE